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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4450_Библиотеки_им_академика_М_И_Перельмана
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premaxillae and the anterior part of the vomeral lamellae
(see ▶ Fig. 1.41).
Fig. 1.113Growth of cartilaginous septum, perpendicular plate, and septum as a whole
between 0 and 20 years. In contrast to body length, there is no growth spurt of the
septum in puberty. (After [195].)
Fig. 1.114Growth of cartilaginous septum, perpendicular plate, and septum as a whole
between 0 and 70 years. (After [195].)
Perpendicular Plate
The perpendicular plate is formed by intracartilaginous
ossification of the cranial and posterior part of the
cartilaginous septum (▶ Fig. 1.115 and ▶ Fig. 1.116). This
process starts in the sixth month in the region of the crista
galli, and slowly proceeds in a caudal and anterior
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direction. Growth of the perpendicular plate continues at a
fast pace until the age of 10 years. It then slows down but
continues until approximately the age of 40 years (▶ Fig.
1.113 and ▶ Fig. 1.114). At puberty, the process of
ossification has reached the vomer. A small strip of
cartilage from the cartilaginous septum remains between
the perpendicular plate and the vomer, the so-called
sphenoidal process of the cartilaginous septum (▶ Fig.
1.117).
Fig. 1.115Ossification of the perpendicular plate and vomer at about 1 to 3 years.
Fig. 1.116Ossification of the perpendicular plate and vomer at about 10 to 17 years.
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Fig. 1.117Sphenoidal process of the cartilaginous septum.
Vomer
The vomer ossifies by intramembranous ossification
between the 12th postovulatory week and birth. The
ossification process takes place from caudal to cranial. Two
lamellae are formed. The cranial–anterior parts of these
lamellae are V-shaped and hold the posterior part of the
cartilaginous septum. The posterior parts or alae enclose
the rostrum sphenoidale. At 6 to 8 years of age, the
perpendicular plate and vomer fuse. Around puberty, the
vomer meets the premaxilla.
Premaxilla
The premaxilla, previously called the intermaxillary bone
(see blue box), is formed by two ossification centers that
emerge at about 8 to 9 weeks of age. They fuse about 1
week later. Then, from the posterior part of the cranial half,
a wing starts to develop on both sides. These premaxillary
alae continue to grow throughout childhood and
particularly during puberty. The premaxilla fuses with the
maxillary bones in the first year of life. Later in puberty, it
fuses with the anterior end of the vomer. Since this is
where the upper incisor teeth develop, early trauma to this
area may lead to irregularities in the position or eruption of
the upper teeth.
The intermaxillary bone was a topic of fierce debate in the
second half of the 18th century. The leading anatomists of
the time, in particular Petrus Camper of Groningen, were of
the opinion that the intermaxillary bone is missing in
humans. In this respect, humans were believed to differ from
the great apes and all higher developed mammals. The
“missing intermaxillary bone” was generally accepted as
proof that humans were created by God and had not
descended from the apes. It was Goethe who, in 1783,
discovered that the intermaxillary bone is present in humans
too but fuses with the maxillary bones.
(Hellmich and Hellmich, 1982)
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Cartilaginous Vault
The triangular cartilages originally extend under the nasal
bones up to the roof of the ethmoid bone (▶ Fig. 1.111).
Their cranial margins lose their connection with the
anterior skull base and gradually retreat in a caudal
direction. By adulthood, they still underlap the bony vault
by 2 to 5 mm (see ▶ Fig. 1.20).
Bony Vault
The medial part of the bony pyramid originates from
intracartilaginous ossification of the upper part of the
cartilaginous nasal capsule. Its lateral part is the result of
ossification of the nasal process of the maxillary bones. In
adult life, the nasal bones partially fuse in the midline.
1.3.4Disturbance of Development and
Growth—Consequences for Nasal
Pathology and Surgery
Disturbance of Nasal Development
Genetic and exogenic factors may interfere with nasal
morphogenesis in many ways. The most well known
malformations are discussed next.
Cleft Lip and Palate
Incomplete fusion of the maxillary process and the lateral
nasal process results in a unilateral or bilateral cleft lip
and/or palate. It is associated with characteristic
deformities of the nasal pyramid, lobule, septum,
turbinates, and nasal cavity (as described in Chapter ▶ 2
and illustrated in ▶ Fig. 2.26, ▶ Fig. 2.27, ▶ Fig. 2.28, ▶ Fig. 2.29,
▶ Fig. 2.30, and ▶ Fig. 2.31). The disturbance of growth that
leads to this malformation occurs in the second month of
embryonic life (see ▶ Fig. 1.108). The earlier the
embryologic development becomes distorted, the more
severe the anomaly.
Nasal Bifidity
Incomplete fusion of the two medial nasal processes causes
bifidity of the nose. This malformation may vary from a
minor vertical groove in the columella or between the two
domes to severe bifidity of the lobule and the cartilaginous
and bony vault (see ▶ Fig. 2.27).
Medial Nasal Fistula, Cyst, and Glioma
Incomplete fusion of the two medial nasal processes may
allow squamous epithelium and brain tissue to become
entrapped in the midline. This may result in a medial nasal
cyst and a fistula extending endocranially. Another wellknown consequence of this developmental disturbance is a
nasal glioma.
Nasal Proboscis
The whole nose or one half of it consists of a russel-like
structure, usually involving the eye and its adnexa. This
serious malformation results from a lesion of the olfactory
plate and/or the forebrain at or before the fifth
postovulatory week.
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Nasal Agenesis
Nasal agenesis is a very rare anomaly in which the external
nose does not develop and the nasal cavity is totally or
partially obliterated.
Choanal Atresia
The choanae are obliterated by a membrane, a bony
lamella, or a combination of the two. The obliterating bony
lamella is part of the palatine bone and usually runs
upward at a slightly oblique angle.
Nasal and Midface Hypoplasia
For reasons that usually remain obscure, the nasal pyramid
and midface do not develop normally. The external nose is
small in all its dimensions and the midface is retruded. The
condition is described in Chapter ▶ 2 (▶ Fig. 2.32, ▶ Fig. 2.33,
▶ Fig. 2.34; ▶ Congenital Nasal Hypoplasia (Nasomaxillary
Dysplasia, Binder Syndrome)).
Disturbance of Nasal Growth
Several events may interfere with the growth of the nose in
a more or less serious way. The most well known factors
are discussed next.
Intrauterine Growth Disturbance
Although relatively rare, nasal growth may be disturbed
during intrauterine life. The congenitally deviated nose is
the most, well-documented example (see ▶ Fig. 9.1).
Birth Trauma
Vaginal birth causes some kind of deformation of the
external nose and septum in a fairly large proportion of
neonates. In most cases, the deformity is corrected
spontaneously as a result of the elasticity of the tissues. In
some children, however, it leads to a deviated septalpyramid syndrome or a low-wide pyramid syndrome in later
life (see Chapter ▶ 2, ▶ Low-Wide Pyramid Syndrome (Saddle
Nose)).
Childhood Trauma
The primary cause of a large percentage of nasal
deformities seen in adults is (repeated) trauma of the
septum and/or external pyramid in early childhood. The
most common late consequences are a deviated nose and
an underdeveloped pyramid and midface. These effects
have been clearly documented in studies on identical twins
by [140], [245], and [91]. The earlier (and the more
destructive) the trauma, the more severe the growth
disturbance and the ultimate nasal pathology.
Childhood Septal Abscess
A septal abscess in childhood poses the greatest threat to
normal nasal growth. Unless treated by septal
reconstruction as soon as possible, it will lead to severe
disturbance of the outgrowth of the septum, pyramid, and
midface. A characteristic example of the growth
disturbance caused by trauma and septal abscess in
childhood is presented in ▶ Fig. 1.118.
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